Plasmodium falciparum kelch13 mutations that cause artemisinin resistant malaria in Southeast Asia show markedly different patterns of evolutionary selection in Africa.

The dominant targets of host immune response to malaria are repeat elements, which are short stretches of amino acids repeated within Plasmodium falciparum proteins, and these are associated with short-lived and exposure-dependent antibody responses.

Ribosome profiling has bridged the knowledge gap between transcription and translation during malaria blood stage development and provided a comprehensive gene expression resource for this parasite.

Plasmodium falciparum aminopeptidase PfA-M17 is essential to parasite survival and plays a role in hemoglobin digestion, providing a rationale for further development of inhibitors against this enzyme.

Controlled human malaria infection model allows the study of gametocyte biology and dynamics providing novel insights and tools in malaria transmission and elimination efforts.

The molecular mechanism behind how emetine inhibits the ribosome of the human malaria parasite, along with structural details of the complex formed, is revealed at high resolution using cryo-electron microscopy.

An enhanced bioinformatic pipeline to quantify Plasmodium falciparum core gene and polymorphic var gene expression revealed changes occurring during early culture adaptation of parasites from naturally infected individuals.

Identifying and treating those groups of individuals that are most likely to transmit the malaria parasite to mosquitoes could help to control the spread of the disease.

The pyruvate kinase contained in the apicoplast organelle of malaria parasites makes the nucleotide triphosphates required for several processes including transcription of the organellar genome.

The first comprehensive analysis of antigenic switching in the malaria-causing parasite Plasmodium falciparum provides new insights into the process that prevents individuals from acquiring immunity to the disease.